ReviewJournal of advanced research2023
Alzheimer's disease and synapse Loss: What can we learn from induced pluripotent stem Cells?
Review in Journal of advanced research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed.
- The Machine Learning Classification of Retinal Ganglion Cell Dendritic Texture in a 3xTg-Alzheimer's Disease Mouse Model.Diagnostics (Basel, Switzerland) · 2026Article
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- Licochalcone a enhances cognitive resilience in APP/PS1 Mice by modulating glucose metabolism, Aβ burden, and neuroinflammation.GeroScience · 2026Article
- Targeting Pain and Depression in Alzheimer's Disease: Translational Insights and Emerging Treatments.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Amyloid-β and Tau in Alzheimer's disease: pathogenesis, mechanisms, and interplay.Cell death & disease · 2026Review
- Roles of Glia in Synapse Nano-organization.Advances in neurobiology · 2026Review
- Cerebrospinal fluid neuronal pentraxin levels are associated with tau pathology via microglia-astrocyte signaling in alzheimer's disease.Journal of neuroinflammation · 2025Article
- ApoE4 Upregulates GSK-3β to Aggravate Alzheimer-Like Pathologies and Cognitive Impairment in Type 2 Diabetic Mice.CNS neuroscience & therapeutics · 2025Article
- Unveiling the therapeutic potential of natural products in Alzheimer's disease: insights fromFrontiers in pharmacology · 2025Review
- Alzheimer's Disease: The Current and Emerging Treatment Approaches.Behavioural neurology · 2025Review
- Computational Design of Novel Tau-Tubulin Kinase 1 Inhibitors for Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Review on anti-alzheimer drug development: approaches, challenges and perspectives.RSC advances · 2024Review
- Modifying Alzheimer's disease pathophysiology with photobiomodulation: model, evidence, and future with EEG-guided intervention.Frontiers in neurology · 2024Review
- Cyanidin-3-O-glucoside protects the brain and improves cognitive function in APPswe/PS1ΔE9 transgenic mice model.Journal of neuroinflammation · 2023Article
- Amyloid-β: A potential mediator of aging-related vascular pathologies.Vascular pharmacology · 2023Review
- Development of a three-dimensional organoid model to explore early retinal phenotypes associated with Alzheimer's disease.Scientific reports · 2023Article
- Going beyond established model systems of Alzheimer's disease: companion animals provide novel insights into the neurobiology of aging.Communications biology · 2023Review
- Alzheimer's Disease Treatment: The Search for a Breakthrough.Medicina (Kaunas, Lithuania) · 2023Review
- Development of brain organoid technology derived from iPSC for the neurodegenerative disease modelling: a glance through.Frontiers in molecular neuroscience · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSynaptic dysfunction is a major contributor to Alzheimeŕs disease (AD) pathogenesis in addition to the formation of neuritic β-amyloid plaques and neurofibrillary tangles of hyperphosphorylated Tau protein. However, how these features contribute to synaptic dysfunction and axonal loss remains unclear. While years of considerable effort have been devoted to gaining an improved understanding of this devastating disease, the unavailability of patient-derived tissues, considerable genetic heterogeneity, and lack of animal models that faithfully recapitulate human AD have hampered the development of effective treatment options. Ongoing progress in human induced pluripotent stem cell (hiPSC) technology has permitted the derivation of patient- and disease-specific stem cells with unlimited self-renewal capacity. These cells can differentiate into AD-affected cell types, which support studies of disease mechanisms, drug discovery, and the development of cell replacement therapies in traditional and advanced cell culture models. AIM OF REVIEW: To summarize current hiPSC-based AD models, highlighting the associated achievements and challenges with a primary focus on neuron and synapse loss. KEY SCIENTIFIC CONCEPTS OF REVIEW: We aim to identify how hiPSC models can contribute to understanding AD-associated synaptic dysfunction and axonal loss. hiPSC-derived neural cells, astrocytes, and microglia, as well as more sophisticated cellular organoids, may represent reliable models to investigate AD and identify early markers of AD-associated neural degeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.